다형성교모세포종 세포주와 종양조직에서 Midkine 발현
Midkine Expression in Cell Lines and Tumor Tissues of Glioblastoma Multiforme
대한암학회지 1999년 31권 3호 p.617 ~ 626
장진우, 라선영, 정상섭, Frank Czubayko, 정현철,
소속 상세정보
장진우 ( Chang Jin-Woo )
Yonsei University College of Medicine Department of Neurosurgery
라선영 ( Rha Sun-Young )
Yonsei University College of Medicine Department of Internal Medicine
정상섭 ( Chung Sang-Sup )
CHA University Bundang CHA Hospital Department of Neurosurgery
( Frank Czubayko )
USA Georgetown University School of Medicine Department of Lombardi Cancer Center
정현철 ( Chung Hyun-Cheol )
Yonsei University College of Medicine Department of Internal Medicine
KMID : 0360319990310030617
Abstract
PURPOSE: We measured the expression of midkine (MK) gene and biophenotypes in brain tumor cell lines and tumor tissues.
MATERIALS AND METHODS: We used the cell lines purchased from ATCC: two glioblastoma cell lines (T98G, U87MG), rat bladder tumor cell line (NBT-II), NIH/3T3, and two endothelial cell lines [(human umbilical vein endothelial cell (HUVEC) and fetal bovine heart endothelial cell (FBHE)]. RNA was taken from 4 cancer tissues of glioblastoma multiforme. Tissue cytosol was obtained from 5 cancer patients and 2 tissues of epilepsy patients. Pentosanpolysulfate(PPS) was used as a competitive inhibitor of heparin-binding growth factor (HBGF). MK and pleiotrophin (PTN) mRNA expression was tested by Northem hybridization, uPA and PAI-1 levels were measured by ELISA (Monozyme, Netherlands). Cross-feeding assay was done to measure the activity of endothelial cell growth stimulation induced by cancer cell lines.
RESULTS: T98G cell line expressed both MK and PTN while U87MG expressed only PTN. In cross-feeding assay, endothelial cell growth increased in proportion to the number of administered feeding tumor cells, T98G and U87MG. This phenomenon was found in HUVEC, but not in FBHE. Conditioned media of T98G and U87MG showed similar stimulatory effect on the growth of NIH/3T3 cells. T98G cell showed higher excretion rate of uPA into conditioned media while U87MG showed higher excretion rate of PAI-1 into conditioned media. 20% of growth inhibition was induced on T98G cell with 100 pg/ml PPS, while 40% of growth inhibition was induced with 10 pg/ml PPS on U87MG cell. In four cancer tissues, thee expressed MK. In cancer tissue cytosol, uPA and PAI-1 expressions varied in individuals. No PAI-1 was found in non-tumor tissues.
CONCLUSION: MK expression was found in brain tumor cell lines and tumor tissues. Modulation of biophenotypes (angiogenic activity and growth) by PPS in tumor cells with MK expression suggested a possible biotherapy in brain tumor targeting growth factor.
키워드
Brain tumor; Midkine; Pentosanpolysulfate; Angiogenic activity;
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